ライフサイエンスコーパス: imatinib

1 ash (ten [6%] of 154 vs two [1%] of 152 with imatinib).

2 e frequently with dasatinib (28% v 0.8% with imatinib).

3 f either Hsp90 (geldanamycin) or Abl kinase (imatinib).

4 Dutch GIST registry treated with neoadjuvant imatinib.

5 ABL tyrosine kinase inhibitors, for example, Imatinib.

6 lowed by ponatinib > bosutinib > dasatinib > imatinib.

7 py results in longer survival than 1 year of imatinib.

8 chronic phase (CP) treated with dasatinib or imatinib.

9 ent occurred in three or more patients given imatinib.

10 ib and 95 patients were randomly assigned to imatinib.

11 r later TKIs and intolerant or refractory to imatinib.

12 nded well after initiation of treatment with imatinib.

13 ranscripts regularly observed in patients on imatinib.

14 rs (GISTs) treated with surgery and adjuvant imatinib.

15 e allocated nilotinib and 320 were allocated imatinib.

16 and patients, associate with sensitivity to Imatinib.

17 valuate for an early response to neoadjuvant imatinib.

18 it most from the longer duration of adjuvant imatinib.

19 e disease in a patient who had received only imatinib.

20 d neoplasms has been dramatically altered by imatinib.

21 ts who had been randomly assigned to receive imatinib.

22 nib, compared with CML patients treated with imatinib.

23 ents with suboptimal cytogenetic response on imatinib.

24 ificantly higher for dasatinib compared with imatinib.

25 n treated with the tyrosine kinase inhibitor imatinib.

26 patients, positive for EBF1-PDGFRB, received imatinib; 1 died 6 months after a matched unrelated bone

27 analysis included 483 patients, 271 received imatinib, 105 received nilotinib, and 107 received dasat

28 ce of iron deficiency by dichloroacetate and imatinib, 2 putative treatments explored for pulmonary a

29 pants received half their standard TKI dose (imatinib 200 mg daily, dasatinib 50 mg daily, or nilotin

30 (IC50 values) on day 6 were 6.06 microM for imatinib, 3.72 microM for dasatinib, and 81.35 microM fo

31 cts with clinically-defined HES who received imatinib (300-400 mg daily >/= 1 month) were classified

32 included 482 patients who were treated with imatinib 400 mg daily (n=68), imatinib 800 mg daily (n=2

33 atients were randomly assigned to 2 years of imatinib 400 mg daily or no further therapy after surger

34 survival significantly differed between the imatinib 400 mg group and the other TKI groups (imatinib

35 ive dasatinib 100 mg once daily (n = 259) or imatinib 400 mg once daily (n = 260).

36 nt, all patients had received 3-18 months of imatinib 400 mg once daily and had a suboptimal cytogene

37 :1) via a randomisation list to receive oral imatinib 400 mg once daily or oral nilotinib 400 mg twic

38 ies were randomly assigned to receive either imatinib 400 mg or 800 mg daily.

39 ete cytogenetic response (58 [87%] of 67 for imatinib 400 mg vs 180 [90%] of 199 for imatinib 800 mg,

40 28 (41%) patients receiving imatinib 400 mg, 85 (43%) receiving imatinib 800 mg, 23

41 for better event-free survival compared with imatinib 400 mg, but that failure-free, transformation-f

42 system to receive oral ponatinib (45 mg) or imatinib (400 mg) once daily until progression, unaccept

43 d after the start of oral administration of imatinib (400 mg/d).

44 All started treatment with imatinib 600 mg/day.

45 CR-ABL1 </= 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progression-free and ove

46 years, respectively) than in those receiving imatinib (8 per 1000 person-years), although data are li

47 ltivariate analysis showed that therapy with imatinib 800 mg (HR 0.51, 95% CI 0.29-0.88, p=0.016), da

48 e treated with imatinib 400 mg daily (n=68), imatinib 800 mg daily (n=200), dasatinib 50 mg twice dai

49 More patients receiving imatinib 800 mg or second-generation TKIs (ie, dasatinib

50 Treatment with imatinib 800 mg or the second-generation TKIs dasatinib

51 tinib 400 mg group and the other TKI groups (imatinib 800 mg p=0.029, dasatinib p=0.003, nilotinib p=

52 Results with imatinib 800 mg were similar to those with second-genera

53 eceiving imatinib 400 mg, 85 (43%) receiving imatinib 800 mg, 23 (21%) receiving dasatinib, and 27 (2

54 for imatinib 400 mg vs 180 [90%] of 199 for imatinib 800 mg, vs 100 [96%] of 104 for dasatinib vs 99

55 was performed at day 22 and if <1000 ng/mL, imatinib 800 mg/day was given.

56 t 1 patients failing any target escalated to imatinib 800 mg/day, and subsequently switched to niloti

57 of-principle trial to evaluate the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness

58 Imatinib, a selective BCR-ABL1 kinase inhibitor, improve

59 Imatinib, a selective inhibitor of platelet-derived grow

60 hase with suboptimal cytogenetic response to imatinib according to the 2009 European LeukemiaNet crit

61 Imatinib administration during 6-7 d increased PTF from

62 Some mice were given the RTK inhibitor imatinib after injection of cancer cells; tumor growth w

63 isease in spite of continuous treatment with imatinib, all of them achieved sustained CMR, up to 4.7

64 zotinib and imatinib was more effective than imatinib alone in imatinib-sensitive GIST models.

65 Imatinib also reduced levels of serum tryptase, a marker

66 ent tissues and driving development of novel imatinib analogs.

67 hese chiral tertiary piperazines resulted in imatinib analogues which exhibited comparable antiprolif

68 tween December 2004 and October 2008: 454 to imatinib and 454 to observation.

69 The patient was treated with imatinib and achieved complete clinical remission of his

70 m of this study was to assess the effects of imatinib and anakinra on PTF and TBF in colorectal cance

71 BCR-ABL tyrosine kinase inhibitors (TKIs) imatinib and dasatinib inhibit fludarabine and cytarabin

72 Importantly, imatinib and nilotinib increased tyrosine phosphorylatio

73 We investigated the effects of imatinib and nilotinib on human NK cells, monocytes, and

74 bition of FAK activity both strongly reduced imatinib and nilotinib stimulated invasion.

75 Imatinib and nilotinib treatment increased two dimension

76 Imatinib and nilotinib-induced tyrosine phosphorylation

77 useful in patients who develop resistance to imatinib and other TKIs used to treat this disease.

78 Imatinib and other tyrosine kinase inhibitors (TKI) have

79 a effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias ex

80 oblastoma multiforme (GBM) tumour cells with imatinib and the closely-related drug, nilotinib, striki

81 We also show that combination treatment with imatinib and tigecycline, an antibiotic that inhibits mi

82 Combining a tyrosine kinase inhibitor (imatinib) and a thiazolidinedione (pioglitazone) is prop

83 ell line (EA.hy926 cells) and pharmacologic (imatinib) and genetic (short hairpin RNA knockdown of IL

84 vy metal drugs (cisplatin), targeted agents (imatinib), and cytotoxic agents (docetaxel).

85 At 2 years, 55% of patients remained on imatinib, and 30% on nilotinib.

86 d to imatinib completed study treatment with imatinib, and 82.8% had a complete cytogenetic response.

87 ese effects were absent in rats treated with imatinib, another BCR-ABL tyrosine kinase inhibitor.

88 RFS remained superior in the imatinib arm (hazard ratio, 0.6; 95% CI, 0.43 to 0.75; C

89 -up of 4.7 years, 5-year IFFS was 87% in the imatinib arm versus 84% in the control arm (hazard ratio

90 n 5% and 7% of patients in the dasatinib and imatinib arms, respectively.

91 the efficacy and safety of nilotinib versus imatinib as first-line therapy for patients with advance

92 p in patients with CML who were treated with imatinib as initial therapy.

93 se inhibitors, including the anticancer drug imatinib, as inhibitors of both SARS-CoV and MERS-CoV in

94 ed that the coadministration of lapatinib or imatinib at clinical doses could result in a significant

95 Despite the success of imatinib at inhibiting Bcr-Abl and treating chronic myel

96 ith more arterial occlusive events than with imatinib at the doses studied.

97 These findings demonstrate that imatinib attenuates multiple cytoskeletal changes associ

98 supports the feasibility and efficacy of an imatinib-based approach with selective, early switching

99 Adjuvant therapy with imatinib benefits patients with a high risk of recurrenc

100 ase inhibitors, such as the anti-cancer drug Imatinib, bind.

101 novel c-Src allosteric sites associated with imatinib binding and kinase activation and provide a fra

102 n functional regulatory sites, distal to the imatinib binding pocket, show similarities to structural

103 Our results demonstrate that imatinib binding to the kinase domain effects dynamics o

104 y GIST patients respond to the Kit inhibitor imatinib, but this drug often becomes ineffective becaus

105 In particular, the resistance to imatinib caused by the gatekeeper mutation T315I in Bcr-

106 high doses of the tyrosine kinase inhibitor imatinib combined with reduced-intensity chemotherapy (a

107 ts (48.3%) who had been randomly assigned to imatinib completed study treatment with imatinib, and 82

108 hase chronic myeloid leukaemia compared with imatinib could not be assessed due to trial termination,

109 tive activity to that of their corresponding imatinib counterparts.

110 ast decade, several targeted therapies (e.g. imatinib, dasatinib, nilotinib) have been developed to t

111 In patients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell

112 apoptosis in a dose-dependent manner, while imatinib did not.

113 different from baseline 1 wk after the last imatinib dosage.

114 ty and efficacy of switching to nilotinib vs imatinib dose escalation for patients with suboptimal cy

115 ponses with switching to nilotinib than with imatinib dose escalation, although the difference was no

116 nib 400 mg twice per day or an escalation of imatinib dose to 600 mg once per day (block size of 4).

117 (ALL) in the elderly has improved during the imatinib era.

118 Whereas imatinib exhibits a well-documented and favorable long-t

119 of the OS benefit derives from the fact that imatinib facilitates alloHSCT.

120 ed GIST, we changed the primary end point to imatinib failure-free survival (IFFS), with agreement of

121 currence were randomized to receive adjuvant imatinib for 1 or 3 years.

122 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has b

123 NK cells and monocytes of patients receiving imatinib for chronic myeloid leukemia.

124 e patients were randomly assigned to receive imatinib for either 1 or 3 years.

125 namics, in the presence and absence of bound imatinib, for full-length human c-Src using hydrogen-deu

126 s-intensive chemotherapy, both combined with imatinib, for patients with newly diagnosed Philadelphia

127 Imatinib (Gleevec), a non-receptor tyrosine kinase inhib

128 p (50%, 95.18% CI 40-61) and 40 of 95 in the imatinib group (42%, 32-53%; difference 7.9% in favour o

129 progression-free survival was higher in the imatinib group (59.2% [95% CI 50.9-66.5]) than in the ni

130 nib group and 34 (36%) of 95 patients in the imatinib group achieved complete cytogenic response at 6

131 nse at 12 months, as only 13 patients in the imatinib group and ten patients in the ponatinib group c

132 and hypophosphatemia were more common in the imatinib group than in the placebo group.

133 th groups was abdominal pain (11 [4%] in the imatinib group, 14 [4%] in the nilotinib group).

134 (+/-SD) of 1.73+/-0.60 doubling doses in the imatinib group, as compared with 1.07+/-0.60 doubling do

135 In the imatinib group, grade 3 or 4 adverse events observed in

136 QT prolongation (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%, after crossover to nilotinib]).

137 last cell crisis (nilotinib group, n=1 [1%]; imatinib group, n=1 [1%]), and QT prolongation (nilotini

138 %, including 1 after crossover to imatinib]; imatinib group, n=1 [1%]), blast cell crisis (nilotinib

139 Among the patients in the imatinib group, the estimated overall survival rate at 1

140 In the imatinib group, the most common grade 3-4 adverse events

141 b group and nine (10%) of 93 patients in the imatinib group.

142 oup and five (5%) of 93 patients died in the imatinib group; no deaths were treatment-related.

143 natinib and three (2%) of 152 patients given imatinib had arterial occlusive events (p=0.052); arteri

144 This study confirms that adjuvant imatinib has an overt impact on RFS.

145 tion of ABL1 kinase inhibitors (for example, imatinib) has markedly improved patient survival, but ac

146 ccount showed a modest additional benefit to imatinib (hazard ratio for EFS = 0.64, 95% confidence in

147 However, the Az and imatinib hybrids have weak inhibitory activities towards

148 d-intensity chemotherapy (arm A) to standard imatinib/hyperCVAD (cyclophosphamide/vincristine/doxorub

149 Purpose Imatinib (IM) can safely be discontinued in patients wit

150 oup, n=2 [2%, including 1 after crossover to imatinib]; imatinib group, n=1 [1%]), blast cell crisis

151 reatment of the first patient with GIST with imatinib in 2000).

152 cript level measured 3 months after starting imatinib in a cohort of 40 children with CML.

153 The Evaluation of Ponatinib versus Imatinib in Chronic Myeloid Leukemia (EPIC) study was a

154 Given the safety of imatinib in humans, plans are underway for pilot clinica

155 ic and recurrent tumors after treatment with Imatinib in most cases a decrease in size and contrast e

156 inhibitor, was markedly more effective than imatinib in multiple preclinical models of imatinib-sens

157 (OR, 3.47; 95% CI, 1.23-9.78) compared with imatinib in patients with CML.

158 400 mg/d) versus a higher dose (800 mg/d) of imatinib in patients with metastatic or locally advanced

159 -blind, placebo-controlled, 24-week trial of imatinib in patients with poorly controlled severe asthm

160 combining reduced-intensity chemotherapy and imatinib in Ph+ ALL adult patients and suggests that SCT

161 ld result in superior outcomes compared with imatinib in previously untreated patients with chronic m

162 explain the failure of Abl kinase inhibitor imatinib in prostate cancer clinical trials.

163 t 2 PAH-specific medications enrolled in the Imatinib in Pulmonary Arterial Hypertension, a Randomize

164 hibitors (pre-TKI) and after introduction of imatinib (in the European Study for Philadelphia-Acute L

165 eginning of the learning curve of the use of imatinib, in a large population of patients with advance

166 icacy and safety of ponatinib, compared with imatinib, in newly diagnosed patients with chronic-phase

167 facilitates elimination of CML stem cells by Imatinib, in part via p53 activation.

168 Imatinib increases PTF of colorectal cancer metastases i

169 g, and significantly dampened sensitivity to Imatinib-induced erythroid differentiation.

170 ion-regulated kinase 1A was shown to enhance imatinib-induced gastrointestinal stromal tumor cell dea

171 Targeting the DREAM complex and imatinib-induced quiescence could provide opportunities

172 onstrated that the tyrosine kinase inhibitor imatinib induces lysosome acidification and antimicrobia

173 known about whether the duration of adjuvant imatinib influences the prognostic significance of KIT p

174 Imatinib inhibited growth of KIT(+) colon cancer organoi

175 Imatinib inhibited hCNT2 with an IC50 value of 2.3 mum P

176 Imatinib-insensitive leukemia stem cells (LSCs) are beli

177 kinase domain in the BCR-ABL fusion protein, imatinib is strikingly effective in the initial stage of

178 sease: imatinib, sunitinib, and regorafenib; imatinib is usually the best tolerated of the three and

179 2B7, 2B15, and 2B17) by four TKIs (axitinib, imatinib, lapatinib and vandetanib) were characterized b

180 ific sarcoma subtype and the availability of imatinib, led to the "Big Bang" of GIST therapy (ie, the

181 uzumab, bendamustine, bortezomib, dasatinib, imatinib, lenalidomide, rituximab alone or in combinatio

182 Lapatinib and imatinib may cause clinically significant DDIs when co-a

183 L stem cell survival and self-renewal during imatinib mesylate (IM) treatment.

184 The PDGF receptor tyrosine kinase inhibitor imatinib mesylate and a monoclonal antibody against PDGF

185 Imatinib mesylate and new TKIs along with allogeneic ste

186 tment of chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or third-generat

187 Imatinib mesylate and other tyrosine kinase inhibitors (

188 Moreover, imatinib mesylate enhanced rat cardiac allograft vasculo

189 ges treated with the selective Abl inhibitor imatinib mesylate had a reduced capability to migrate in

190 act-a phase 2 study demonstrated efficacy of imatinib mesylate in patients with metastatic GIST harbo

191 Treatment of mice with the c-KIT inhibitor imatinib mesylate limited effusion precipitation by mous

192 tworks, differential sensitivity to the drug imatinib mesylate, and differential self-renewal capacit

193 nts were randomized to 1 of 2 dose levels of imatinib mesylate, including 400 mg once daily (400 mg/d

194 mia (CML) occurred after the introduction of imatinib mesylate, the first tyrosine kinase inhibitor (

195 The duration of adjuvant imatinib modifies the risk of GIST recurrence associated

196 IL-3 and serum-starved 32D cells with 1 muM imatinib mysylate inhibited IL-3 stimulated kinase activ

197 mly assigned to receive ponatinib (n=155) or imatinib (n=152).

198 he effects of the tyrosine kinase inhibitors imatinib, nilotinib, and dasatinib on B. malayi adult ma

199 sessed interactions of bosutinib, dasatinib, imatinib, nilotinib, and ponatinib with recombinant hNTs

200 CML patients at diagnosis (n = 21), on TKI (imatinib, nilotinib, dasatinib) before achieving major m

201 CML patients treated with a novel sequential imatinib/nilotinib strategy aimed at achievement of opti

202 o Here we show that the anti-CoV activity of imatinib occurs at the early stages of infection, after

203 The use of imatinib or dasatinib as a c-Kit inhibitor reduced the l

204 d CML in the chronic phase to receive either imatinib or interferon alfa plus cytarabine.

205 hough GISTs are often initially sensitive to imatinib or other tyrosine kinase inhibitors, resistance

206 ased the rate of MMR at 1 year compared with imatinib (overall OR, 2.22; 95% CI, 1.87 to 2.63).

207 atinib and in one (1%) of 152 patients given imatinib (p=0.010).

208 onatinib and five [38%] of 13 patients given imatinib; p=0.074).

209 ars of follow-up showed that the efficacy of imatinib persisted over time and that long-term administ

210 Imatinib plasma trough level was performed at day 22 and

211 ed anaphylaxis with the ABL kinase inhibitor imatinib protected the mice from severe IgE-mediated ana

212 nia (19 [12%] of 154 vs ten [7%] of 152 with imatinib), rash (ten [6%] of 154 vs two [1%] of 152 with

213 However, Abl kinase inhibition by imatinib reduces rapid redistribution of the important c

214 subset of human GIST specimens that acquired imatinib resistance acquired expression of activated for

215 f low-level BCR-ABL1 mutations present after imatinib resistance has prognostic significance for subs

216 dentified known and new mutations conferring imatinib resistance in chronic myeloid leukemia cells.

217 CL1 combination, which was also effective in imatinib-resistant cells.

218 In imatinib-resistant GIST with a secondary Kit mutation, K

219 preclinical models of imatinib-sensitive and imatinib-resistant GIST.

220 n, and may offer a new strategy for treating imatinib-resistant GISTs.

221 inib or RNA interference was cytotoxic to an imatinib-resistant human GIST cell population.

222 Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut)) become fully auto-phos

223 I3K and MEK inhibition was effective against imatinib-resistant Kit(V558Delta;T669I/+) tumors.

224 However, imatinib-resistant mutations are increasingly prevalent

225 r responses in both previously untreated and imatinib-resistant patients with CML.

226 bserved with nilotinib/dasatinib therapy for imatinib-resistant patients with multiple mutations were

227 e data also identify imatinib-sensitive, and imatinib-resistant, mutation sites.

228 LSCs, aberrantly expressed proteins, in both imatinib-responder and non-responder patients, are modul

229 argeted genes were significantly enriched in Imatinib response gene signatures in cell lines and chro

230 on gene, little is known about predictors of imatinib response in clinically-defined hypereosinophili

231 Clinical features of MHES predict imatinib response in PDGFRA-negative HES.

232 Overall, imatinib response rates were 100% in the FP group (n = 1

233 rapeutic interventions toward more efficient imatinib responses.

234 A biosynthesis, where pathway inhibition via imatinib results in marked PPP impairment and an accumul

235 characteristic intracellular accumulation of imatinib-sensitive and -resistant Kit protein is well do

236 n imatinib in multiple preclinical models of imatinib-sensitive and imatinib-resistant GIST.

237 Both imatinib-sensitive and imatinib-resistant Kit (Kit(mut))

238 ib was more effective than imatinib alone in imatinib-sensitive GIST models.

239 MET activation also occurred in imatinib-sensitive human GIST cell lines after imatinib

240 These data also identify imatinib-sensitive, and imatinib-resistant, mutation sit

241 tumors such as stage 4 neuroblastomas (NB), imatinib showed benefits that might depend on both on-ta

242 actions built on NCI-60 data identified that Imatinib significantly targeted the NCOR1 governed trans

243 We report the final results of the Stop Imatinib (STIM1) study with a long follow-up.

244 analysis from the phase III Dasatinib Versus Imatinib Study in Treatment-Naive Chronic Myeloid Leukem

245 ologic adverse events (AEs), experience with imatinib suggested that toxicities are typically managea

246 oved for the management of advanced disease: imatinib, sunitinib, and regorafenib; imatinib is usuall

247 gonists currently in clinical use, including imatinib, sunitinib, and sorafenib.

248 CML, with over 80% of patients treated with imatinib surviving for more than 10 years.

249 We specifically identified the imatinib target, Abelson tyrosine-protein kinase 2 (Abl2

250 nd FAK activity and was independent of known imatinib targets including Abl, platelet derived growth

251 ole for NK cells in facilitating response to imatinib that cannot be overcome by subsequent intensifi

252 hod was applied to a three-step synthesis of imatinib, the API of Gleevec, in good yield without the

253 Imatinib, the first and arguably the best targeted thera

254 Imatinib, the first BCR-ABL1 TKI granted regulatory appr

255 Similar to imatinib, the partial response rate for regorafenib by C

256 underexpression predicts a worse response to imatinib, the standard treatment for Ph(+) CML.

257 = 5) were enrolled in a prospective study of imatinib therapy (NCT00044304: registered at clinicaltri

258 Three years of adjuvant imatinib therapy are recommended for patients with GI st

259 Imatinib therapy drives the leukemic population into the

260 MET activation also developed after imatinib therapy in a mouse model of GIST (KitV558del/+

261 Right from the start of Imatinib therapy in inoperable and disseminated GIST pat

262 Three years of adjuvant imatinib therapy results in longer survival than 1 year

263 Neoadjuvant imatinib therapy should be considered for patients requi

264 any patients who otherwise responded well to imatinib therapy still showed variations in their BCR-AB

265 randomized 5-arm trial designed to optimize imatinib therapy, were analyzed for comorbidities at dia

266 e (22 [14%] of 154 vs three [2%] of 152 with imatinib), thrombocytopenia (19 [12%] of 154 vs ten [7%]

267 rexpressing morgana restored the efficacy of imatinib to induce apoptosis, suggesting that ROCK inhib

268 onal dynamics associated with the binding of Imatinib to the proto-oncogene c-Src.

269 rprisingly, immunofluorescence microscopy of imatinib-treated cells revealed a marked colocalization

270 In contrast, no mice in the imatinib-treated control cohorts were cured.

271 Fifteen dasatinib-treated and 19 imatinib-treated patients had BCR-ABL1 mutations identif

272 study closure, 61% and 63% of dasatinib- and imatinib-treated patients remained on initial therapy, r

273 that RNA degradation is inhibited with short imatinib treatment and transcription is inhibited upon l

274 atinib-sensitive human GIST cell lines after imatinib treatment in vitro.

275 gh the BCR-ABL-ERK pathway, and we show that imatinib treatment not only downregulates phosphosites i

276 Furthermore, the absence of SCF or imatinib treatment prevents progenitors from developing

277 the 62 patients who underwent randomization, imatinib treatment reduced airway hyperresponsiveness to

278 ggesting that ROCK inhibitors, combined with imatinib treatment, can overcome suboptimal responses in

279 KIT mutants, including a mutant resistant to imatinib treatment, responded well to a combination of T

280 took place after insulin/IGF1 stimulation or imatinib treatment, suggesting that the direct SHP2-p85

281 ent and transcription is inhibited upon long imatinib treatment, validating the triomics results.

282 Imatinib treatment, which inhibits KIT signaling, deplet

283 BCR-ABL signaling, reducing the efficacy of imatinib treatment.

284 ogenitors are present in patients undergoing imatinib treatment.

285 ces durable, long-term overall survival with imatinib treatment.

286 ty can be partially attenuated by concurrent imatinib treatment.

287 s in the neoplastic tissue of GIST following Imatinib treatment.

288 f gastrointestinal stromal tumors (GISTs) to imatinib treatment.

289 l UGTs (i.e., UGT1A7 by lapatinib; UGT1A1 by imatinib; UGT1A4, 1A7 and 1A9 by axitinib; and UGT1A9 by

290 BL1 kinase remained effectively inhibited by imatinib under hypoxia, apoptosis became partially suppr

291 d an intergroup randomized trial of adjuvant imatinib versus no further therapy after R0-R1 surgery p

292 Imatinib was found to exhibit broad inhibition on severa

293 Moreover, combining crizotinib and imatinib was more effective than imatinib alone in imati

294 er time and that long-term administration of imatinib was not associated with unacceptable cumulative

295 After >/= 18 months in complete remission, imatinib was tapered and discontinued in 8 FP and 1 MHES

296 Imatinib was the first targeted tyrosine kinase inhibito

297 Among 142 long-term survivors, imatinib was the sole therapy administered in 69 (48.6%)

298 cal, molecular, and bone marrow responses to imatinib were assessed.

299 idered by the investigators to be related to imatinib were uncommon and most frequently occurred duri

300 and deeper responses than did standard-dose imatinib, which were maintained after 5 years of follow-